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23 publications mentioning ssc-mir-125b-1

Open access articles that are associated with the species Sus scrofa and mention the gene name mir-125b-1. Click the [+] symbols to view sentences that include the gene name, or the word cloud on the right for a summary.

[+] score: 278
As examples, the liver-specific miR-122 promotes the replication of hepatitis C virus (HCV) [17], [18], while miR-196, miR-199, miR-296, miR-351, miR-431 and miR-448 inhibit HCV genome propagation [19], [20]; miR-32 effectively restricts the accumulation of primate foamy virus type 1 (PFV-1) in human cells [21]; miR-323, miR-491 and miR-654 inhibit the replication of the H1N1 influenza A virus by binding to the viral PB1 gene [22]; miR-28, miR-125b, miR-150, miR-223 and miR-382 target the 3′ end of human immunodeficiency virus (HIV) mRNA, thereby restricting HIV production [23]; miR-199a-3p and miR-210 limit the hepatitis B virus (HBV) surface antigen and polymerase production by degrading and/or inhibiting translation of viral mRNAs encoding these proteins [24]; overexpression of miR-24 and miR-93 suppresses vesicular stomatitis virus (VSV) replication through targeting the viral genes encoding RNA -dependent RNA polymerase (L protein) and phosphoprotein (P protein), respectively [25]; in macrophages, upregulation of miR-155 suppresses VSV replication, while inhibition of miR-155 had the opposite effect. [score:24]
Of note, in addition to acting on κB-Ras2, miR-125b is also predicted (by TargetScan, miRanda and PicTar) to target a number of cellular mRNAs encoding proteins involved in apoptosis and inflammation processes, such as NAIF1 (nuclear apoptosis inducing factor 1), BAK1 (BCL2-antagonist/killer 1), RIT1 (Ras-like without CAAX 1), KSR2 (kinase suppressor of Ras 2), BCL2L12 (BCL2-like 12), and IRF4 (IFN regulatory factor 4), several of which have been validated as miR-125b targets recently [48], [51]– [56]. [score:10]
We found that overexpression of miR-125b stabilized κB-Ras2 mRNA and down-regulated of NF-κB activation in MARC-145 cells (Figure 5), and that pharmacological inhibition of NF-κB impaired PRRSV replication (Figure 6). [score:8]
When we were making efforts to choose potential cellular targets of miR-125b for further study, Murphy et al. reported that miR-125b negatively regulates NF-κB by stabilizing the mRNA encoding κB-Ras2 (NF-κB inhibitor interacting Ras-like 2), a key inhibitor of NF-κB signaling [48]. [score:8]
Because miR-125b does not target directly the PRRSV genome or affect cellular interferon responses, we next reasoned that miR-125b might target other proviral cellular factor(s) to reduce PRRSV replication. [score:6]
PRRSV infection down-regulates the expression of miR-125b, which relieves the stabilizing effect on κB-Ras2 mRNA, resulting in subsequent NF-κB activation. [score:6]
If the PRRSV cDNA insert contains miR-125b target sequence, the expression of luciferase reporter will be subjected to regulation by miR-125b. [score:6]
Consistent with this, ectopic expression of miR-125b mimic upregulated the abundance of κB-Ras2 transcript in MARC-145 cells (Figure 5B), presumably by stabilizing the κB-Ras2 mRNA [48]. [score:6]
As a survival strategy, PRRSV downregulates the expression of miR-125b post-infection and activates NF-κB to facilitate its own multiplication. [score:6]
As shown in Figure 5C, the ecotopically expressed miR-125b mimic down-regulated the basal NF-κB activity in a dose -dependent manner in MARC-145 cells, which was in agreement with the reported effect of miR-125b in human macrophages [48]. [score:6]
Interestingly, we found that PRRSV infection down-regulated the expression of miR-125b as the infection progressed. [score:6]
If that is really the case, PRRSV infection should down-regulate miR-125b expression for its survival advantage. [score:6]
0055838.g007 Figure 7 PRRSV infection down-regulates the expression of miR-125b, which relieves the stabilizing effect on κB-Ras2 mRNA, resulting in subsequent NF-κB activation. [score:6]
In aggregate, these data support the notion that PRRSV infection down-regulates miR-125b to negate the latter’s inhibitory effect on NF-κB, thereby facilitating viral replication. [score:6]
Instead of directly targeting the PRRSV genome, miR-125b exerts it antiviral effect by negatively regulating cellular NF-κB signaling, which we have shown to be a proviral factor for PRRSV replication (Figure 7). [score:5]
miR-125b does not directly target the PRRSV genome. [score:4]
Thus, miR-125b does not appear to directly target the PRRSV genome. [score:4]
We also investigated the underlying mechanism(s) and found that miR-125b does not directly target the PRRSV genome but rather inhibits activation of NF-κB, which is required for optimal replication of PRRSV. [score:4]
miR-125b does not Directly Target the PRRSV Genome. [score:4]
We compared the basal expression levels of miR-125b, miR-155, miR-23a and miR-365 in PAMs by qPCR and found that miR-125b was among the most highly expressed miRNAs examined (data not shown). [score:4]
Significant down-regulation was first observed at 12 h, and further reductions in miR-125b abundance took place at later time points (Figure 6D). [score:4]
Considering that miR-125b negatively regulates NF-κB by stabilizing the mRNA encoding κB-Ras2 in human cells and that PRRSV infection activates NF-κB, we studied the relationship of miR-125b expression, NF-κB activation, and PRRSV replication. [score:4]
In the current study, the reduction of PRRSV replication by miR-125b did not appear to involve direct targeting of the PRRSV genome (Figure 3), nor did it result from activation/augmentation of the IFN response (Figure 4). [score:4]
We determined whether miR-125b specifically targets the PRRSV genome to exert its antiviral effect. [score:3]
0055838.g006 Figure 6 (A) Overexpression of the NF-κB p65 subunit promotes PRRSV replication and partially antagonizes miR-125b’s effect on PRRSV. [score:3]
Conversely, transfection of the miR-125b inhibitor demonstrated the opposite effects (Figure 1B), indicating that miR-125b has antiviral activity against PRRSV replication. [score:3]
To further exclude the possibility that the reduction effects of miR-125b on PRRSV replication resulted from cellular toxicity, MARC-145 cells were transfected with miR-125b mimic or inhibitor at different doses (30 nM, 60 nM, and 120 nM). [score:3]
MicroRNA (miRNA) screening identifies miR-125b as an inhibitor of porcine reproductive and respiratory syndrome virus (PRRSV) replication. [score:3]
The mimics and inhibitors of miR-24, miR-93, miR-122, miR-125b, miR-146a, miR-155, miR-181, miR-196, miR-351, and miR-365 (shown in Table S1) were obtained from GenePharma (Shanghai, China). [score:3]
However, it is important to recognize the possibility that miR-125b may also target other unrecognized cellular factor(s)/pathway(s) pivotal for PRRSV replication as part of it antiviral mechanisms. [score:3]
The miR-125b expression level at 6 h in mock-infected cells was used as the baseline (1.0) for comparison. [score:3]
To screen the potential miRNAs which can reduce PRRSV replication, the mimics or inhibitors of 10 miRNAs (Table S1), including miR-24, miR-93, miR-122, miR-125b, miR-146a, miR-155, miR-181, miR-196, miR-351, and miR-365, were chosen and synthetized. [score:3]
Our results revealed that miR-125b is an inhibitor of PRRSV replication. [score:3]
MARC-145 cells were co -transfected with 0.1 µg of pNF-κB-Luc, 0.05 µg of pRL-TK, and 60 nM of miR-125b mimic (D) or inhibitor (E), followed by PRRSV infection 24 h later. [score:3]
It is plausible to speculate that PRRSV infection gradually decreases miR-125b mRNA expression, which, in turn, relieves the stabilizing effect on κB-Ras2 mRNA, ultimately leading to subsequent NF-κB activation. [score:3]
Conversely, transfection of the miR-125b inhibitor significantly augmented PRRSV -induced NF-κB (Figure 5E). [score:3]
No appreciable effect of either the mimic or inhibitor of miR-125b (at up to 120 nM) on cellular viability and morphology could be observed (data not shown). [score:3]
Because miR-125b is highly conserved among different species, we further determined the effect of miR-125b on PRRSV replication in PAMs, the target cells of PRRSV infection in vivo. [score:3]
Having confirmed that the miR-125b mimic had the desired effect on κB-Ras2 expression, we performed an NF-κB reporter assay to determine if miR-125b negatively regulated NF-κB activation in MARC-145 cells. [score:3]
As predicted, significantly decreased miR-125b expression was first observed at 12 h post PRRSV infection, and the miR-125b abundance was further reduced gradually as the infection progressed. [score:3]
MARC-145 cells were cotransfected with a control vector or vector encoding p65 (1.0 µg) and 60 nM of miR-125b mimic or inhibitor. [score:3]
0055838.g002 Figure 2 (A) Overexpression of miR-125b mimic reduced PRRSV replication in a dose -dependent manner. [score:3]
Importantly, ectopic expression of the miR-125b mimic not only reduced the basal NF-κB activity but also ablated that activated by PRRSV (Figure 5D). [score:3]
Conversely, inhibition of miR-125b substantially enhanced PRRSV propagation (Figure 1). [score:3]
Ectopically expressed miR-125b reduced PRRSV progeny virus production. [score:3]
It has been reported that miR-125b is highly expressed and enriched in macrophages [51]. [score:3]
MARC-145 cells infected with PRRSV at a MOI of 0.1 were collected at the indicated time points and qRT-PCR analysis was performed to detect miR-125b expression. [score:3]
miR-125b Negatively Regulates NF-κB Activation in MARC-145 Cells. [score:2]
miR-125b negatively regulates NF-κB activation. [score:2]
Among the miRNAs tested, the overexpression of miR-125b mimic significantly reduced progeny PRRSV production as determined by plaque assay (Figure 1A). [score:2]
For luciferase reporter gene assay, subconfluent MARC-145 cells cultured in 24-well plates were co -transfected with 100 ng/well of the indicated reporter plasmid and 50 ng/well of pRL-TK (as an internal control to normalize the transfection efficiency, Promega), along with the indicated amount of miR-125b mimic or inhibitor. [score:2]
If miR-125b reduces PRRSV replication by down -regulating NF-κB, activation of NF-κB should promote PRRSV replication. [score:2]
Of note, in the absence of miR-125b mimic, overexpression of p65 also increased PRRSV replication compared to cells transfected with the control vector. [score:2]
The pMIR-REPORT luciferase reporter vector (Ambion) was used as the cloning vector for reporter gene assay analyzing the potential target region of miR-125b in PRRSV genome. [score:2]
Based on the results above and those from previous studies [49], [50], it appears that PRRSV infection induces NF-κB activation, which facilitates PRRSV replication, while miR-125b negatively regulates NF-κB signaling, thereby reducing PRRSV replication. [score:2]
Therefore, we propose a working mo del in which miR-125b negatively regulates NF-κB, thereby reducing PRRSV replication (Figure7). [score:2]
Thus, it is plausible that PRRSV infection activates NF-κB, which, in turn, enhances PRRSV replication, and that miR-125b reduces PRRSV replication by down -regulating NF-κB activation. [score:2]
Viral plaque assays showed that coexpression of p65 partially reversed the reduction effect of miR-125b on PRRSV replication (Figure 6A). [score:2]
To corroborate our findings with miR-125b, MARC-145 cells were transfected with increasing concentrations of miR-125b mimic (30, 60, 120 nM), followed by PRRSV infection for 48 h. Virus plaque assays demonstrated that ectopic expression of miR-125b mimic, but not of a control mimic, reduced PRRSV replication in a dose -dependent manner (Figure 2A). [score:2]
Therefore, we analyzed the temporal kinetics of miR-125b expression in PRRSV infected MARC-145 cells by qPCR (primer sequences shown in Table S2). [score:2]
Collectively, these data demonstrate that miR-125b negatively regulates cellular basal NF-κB activity as well as that induced by PRRSV infection. [score:2]
The Inter-relationship among miR-125b, NF-κB Activation and PRRSV Replication. [score:1]
0055838.g004 Figure 4 (A) MARC-145 cells were co -transfected with IFN-β-Luc, pRL-TK, and 30 nM of miR-125b mimic or NC mimic. [score:1]
These data led us to reason that miR-125b might act on a proviral cellular factor(s)/pathway(s) to reduce PRRSV replication. [score:1]
To test this hypothesis, we first analyzed the 3′UTR sequence of κB-Ras2 for miR-125b and found it was highly conserved between human, monkey and pig (Figure 5A). [score:1]
The relative luciferase activities (miR-125b/NC) refer to fold change in luciferase activity in miR-125b mimic -transfected cells relative to respective NC mimic -transfected controls. [score:1]
Identification of miR-125b as an Antiviral miRNA Against PRRSV Replication. [score:1]
At 48 h post-infection, the miR-125b abundance had decreased to nearly 30% of the pre-infection level (Figure 6D). [score:1]
To test this possibility, MARC-145 cells were co -transfected with the IFN-β luciferase reporter and either miR-125b mimic or NC mimic, followed by mock-stimulation or stimulation by poly(I:C). [score:1]
Whether any of these potential targets are involved in the antiviral program of miR-125b against PRRSV will require future investigation. [score:1]
To this end, MARC-145 cells were co -transfected with the NF-κB luciferase reporter and either miR-125b mimic or NC mimic, followed by PRRSV infection, to detect the NF-κB promoter activity. [score:1]
0055838.g005 Figure 5(A) Alignment of miR-125b sequence with the 3′UTR of human (GenBank accession no. [score:1]
In summary, our data demonstrate that miR-125b is an antiviral host factor that restricts PRRSV replication. [score:1]
Herein, we provide data demonstrating that miR-125b is a novel antiviral host factor against PRRSV, an economically important animal virus that devastates the swine industry worldwide. [score:1]
miR-125b mimic or control mimic was co -transfected with the individual reporter vectors into MARC-145 cells, along with an internal control vector, pRL-TK (to normalize the transfection efficiency). [score:1]
The PAMs were transfected with miR-125b mimic or NC mimic (60 nM), followed by PRRSV infection (MOI = 0.1). [score:1]
Taken together, these data suggest that the antiviral activity of miR-125b does not involve the activation of IFN response. [score:1]
miR-125b reduces PRRSV replication in MARC-145 cells and porcine alveolar macrophages (PAMs). [score:1]
miR-125b does not induce the IFN pathway. [score:1]
Collectively, these data unequivocally confirm that miR-125b reduces PRRSV replication. [score:1]
PAMs were transfected with miR-125b mimic or negative control (60 nM), followed by PRRSV infection (MOI = 0.1). [score:1]
MARC-145 cells were transfected with miR-125b mimic or the control mimic prior to PRRSV infection. [score:1]
As shown in Figure 3B, the relative luciferase activities for different vectors containing various PRRSV cDNA segments were not significantly different between cells transfected with miR-125b mimic and control mimic (Figure 3B). [score:1]
MARC-145 cells were transfected with miR-125b mimic or a control mimic (NC) at the indicated dose (30, 60, 120 nM), followed by PRRSV infection (MOI = 0.1). [score:1]
Because targeting host factors for developing antiviral drugs has the advantage of higher genetic barrier to the emergence of viral escape mutants, the identification and characterization of miR-125 as an inhibitor of PRRSV replication may open new ways of controlling future PRRS outbreaks, for which effective control measures remain scanty. [score:1]
The Anti-viral Effect of miR-125b is Independent of the Interferon (IFN) Pathway. [score:1]
Briefly, MARC-145 cells were transfected with miR-125b mimic or the control mimic prior to PRRSV infection. [score:1]
Thus, it is possible that the antiviral effect of miR-125b against PRRSV resulted from activation of the IFN response. [score:1]
The proposed mo del for the inter-relationship among miR-125b, NF-κB activation and PRRSV replication. [score:1]
The PAMs were transfected with miR-125b mimic or negative control (60 nM), followed by PRRSV infection (MOI = 0.1). [score:1]
The inter-relationship among miR-125b, NF-κB activation and PRRSV replication. [score:1]
The PAMs transfected with miR-125b mimic (60 nM) yielded significantly lower PRRSV titers than those transfected with the control mimic (Figure 2C). [score:1]
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[+] score: 75
Using an integrative screening strategy, Kim et al. [39] found that the negative NF-κB regulator TNFAIP3 is a direct target of miR-125b, which suggested that the presence of a positive self-regulatory loop whereby suppression of TNFAIP3 function by miR-125 could strengthen and prolong NF-κB activity. [score:8]
All raw data and statistical results of these real-time PCR tests are available in Supplementary Document 6. Figure 3 shows that Salmonella inoculation down-regulated miR-125b, miR-221, miR-27b and up-regulated miR-26a. [score:7]
In three of the four cases tested (miR-221/FOS, miR-27b/IFNG and miR-125b/MAPK14), the sites identified by TargetScan influenced expression of an upstream ORF when expressed in the same cells as the corresponding miRNAs. [score:7]
Tili et al. showed that miR-125b targets the 3’ UTR of TNF-α transcripts and therefore its down-regulation in response to LPS may be required for proper TNF-α production [37, 38]. [score:6]
The expression of miR-125b was down-regulated 18-fold at 2 days of Salmonella inoculation (P<0.01). [score:6]
Our results indicated that miR-125b is a direct regulator of the CDC42 effects, and significantly down -regulating miR-125b will release the inhibition of MAPK14 and enhance the downstream MAPK signalling pathway. [score:6]
Interestingly, one of the targets of miR-27b, the MPAK14, is also predicted to target miR-125b, which was described above. [score:5]
LPS stimulation of mouse Raw 264.7 macrophages resulted in the down-regulation of miR-125b levels [37]. [score:4]
Slight differences was observed in the Renilla luciferase signal at 24 h post transfection, and both mutations in the miR-125b binding site of the 3’ UTR of MAPK14 significantly induced expression of the upstream Renilla luciferase. [score:4]
Both mutations in the miR-125b binding site of the 3’ UTR of MAPK14 induced expression of the upstream Renilla luciferase 48 h post transfection. [score:4]
One mutation in the miR-125b binding site in the 3’ UTR of MAPK14 significantly induced expression of the upstream Renilla luciferase at 24 h post transfection. [score:4]
Both mutations in the miR-125b binding site of the 3’ UTR of MAPK14 induced expression of the upstream Renilla luciferase at 48 h post transfection. [score:4]
However, only one gene in the Salmonella infection pathway, MAPK14, was predicted to target miR-125b. [score:3]
Using northern blotting and real-time PCR technology, we found that miR-125b was significantly suppressed in the peripheral blood samples after Salmonella inoculation. [score:3]
It has been reported that the miR-125b plays a role in the innate immune response. [score:1]
The hybridization of miR-145, miR-125b, miR-221 and miR-27b showed signals that were approximately 22 nt in size, whereas the let-7f, miR-142, miR-26a, miR-19b and miR-99a detected not only the mature form but also the approximately 75-nt precursors on the same blots (Figure 2). [score:1]
miR-125b is the most attractive of the miRNA identified in this experiment that involved in the Salmonella infection pathway. [score:1]
This work suggests that a number of miRNAs in the Salmonella infection pathway and miR-221, miR-125b and miR-27b played an important role. [score:1]
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[+] score: 46
From the 22 more expressed miRNAs (>80 reads) in spleen, 7 miRNAs (31.8%) were DE, four up-regulated in virulent ASFV infected animal (miR-92a, miR-126-5p, miR-92c and miR-30e-5p) and 3 down-regulated (miR-125b, miR-451 and miR-125a) (Table  4). [score:9]
Of the 8 differentially expressed miRNAs identified at the same time post-infection in infected animals with the virulent strain compared with animals infected with its attenuated strain, miR-126-5p, miR-92c, miR-92a, miR-30e-5p and miR-500a-5p presented up-regulation whereas miR-125b, miR-451 and miR-125a were down-regulated. [score:8]
Down-regulation of Bcl2 by miR-125b might contribute to the inhibition of the early apoptosis of E75 infected macrophages thus favoring the success of its replication. [score:6]
From the gene network analysis, we found that some miRNAs like miR-451 and miR-145-5p, which are the most represented DE miRNAs in spleen, and are highly up-regulated at 7 dpi, are associated with the viral gene 1242 L. This gene, also regulated by miR-125a and miR-125b, is involved in RNA transcription and processing [50]. [score:5]
miR-125b was DE in spleen at 3 dpi between virulent and attenuated strains, being down-regulated by the virulent E75 strain. [score:4]
Interestingly, the three miRNAs that interact with Bcl2 (miR-23a, miR-125a and miR-125b), do not theoretically regulate A179L, the homologous viral gene of the apoptosis inhibitor gene Bcl2 [53]. [score:4]
Ten miRNAs were selected for target prediction according to the highest representation by tissue and conditions: miR-23a, miR-30e-5p, miR-92a, miR-122, miR-125b, miR-126-5p, miR-145-5p, miR-125a, miR-451 and miR-126-3p. [score:3]
For 7 miRNAs: miR-23a, miR-30e-5p, miR-92a, miR-122, miR-125b, miR-126-5p and miR-125a, significant pathways were found related to immune response such as B and T cell receptor signaling pathway, natural killer cell mediated cytotoxicity or Fc gamma R -mediated phagocytosis and with some processes related to the pathogenesis and virus-host interaction, like desencapsidation, apoptosis inhibition, autophagy or host DNA damage response. [score:3]
Target prediction analysis showed that miR-125b can interact with Bcl2. [score:3]
miR-125b was shown to interact with a large number of genes, thus, some pathways related to immune response have been identified for this miRNA. [score:1]
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[+] score: 28
Looking at the most expressed miRNAs, Ssc-miR-125b and Ssc-miR-99a were up regulated in EU, Hsa-miR-200c-3p and Ssc-miR-192 were up regulated in EA and Hsa-miR-200b-3p, Ssc-miR-23a and Ssc-miR-23b were up regulated in AS. [score:6]
Interestingly, Hsa-miR-200b-3p is the most expressed miRNA in all breeds except for Iberian breed, which Ssc-miR-125b (567 reads), Ssc-miR-99a (339 reads) and Hsa-miR-200b-3p (239 reads) are the first, the second and the third most expressed miRNAs, respectively. [score:5]
As an example, Ssc-miR-125b was the most expressed miRNA in Iberian breed, followed by Ssc-miR-99a and Hsa-miR-200b-3p, and Ssc-miR-192 and Hsa-miR-200c-3p were the fourth and fifth most expressed miRNAs in Large White breed, respectively. [score:5]
miRNA expression profile in kidney revealed that the most expressed miRNAs were Hsa-miR-200b-3p, Ssc-miR-125b and Ssc-miR-23b. [score:5]
The most expressed miRNAs (CN>350, 0.30%) in porcine kidney are listed in Table 3. The most abundant miRNA was Hsa-miR-200b-3p (27,097, representing 23.50% of all porcine kidney miRNAs), followed by Ssc-miR-125b (8,809; 7.64%), Ssc-miR-23b (5,412; 4.69%), Ssc-miR-126 (5,274; 4.57%) and Ssc-miR-23a (5,156; 4.47%). [score:3]
In this sense, variants expression followed two main patterns: according to those miRNAs with more than 1,000 total reads, they were distributed in those miRNAs with a strong predominant isomiR, such as Hsa-miR-200b-3p, Ssc-miR-125b, Ssc-miR-23b, Ssc-miR-23a, Ssc-miR-192, Ssc-miR-10b, Ssc-miR-126* and Ssc-miR-10a, and those miRNAs where there is not a really strong predominant isomiR, like Ssc-miR-126, Ssc-miR-99a, Hsa-miR-200c-3p, Ssc-miR-30d and Ssc-miR-125a (Table S3). [score:3]
The miRNA with more variants was Hsa-miR-200b-3p with 123 variants, followed by Ssc-miR-23b and Ssc-miR-125b, with 59 and 51 variants, respectively. [score:1]
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[+] score: 26
Thus it was speculated that PRRSV infections induce the down-regulation of miR-125b, which subsequently results in increased κB-RAS2 expression and ultimately reduced NFκB expression. [score:8]
The reduction was attributed to increased NFκB due to the decreased expression of the negative regulator κB-RAS2, a miR-125 target gene. [score:6]
The cellular miRNA miR-125b was found to be down-regulated in PRRSV-infected cells [7]. [score:4]
This reduction in viral replication was attributed to the modulation of NFκB expression by miR-125b. [score:3]
MiR-125b targets κB-RAS2 which serves as a negative regulator of NFκB. [score:3]
PRRSV replication was also reduced in MARC-145 cells transfected with a miR-125 mimic [7]. [score:1]
of a miR-125b mimic into MARC-145 cells, a PRRSV permissive cell line, resulted in reduced PRRSV replication [7]. [score:1]
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[+] score: 14
In this sense, many porcine miRNAs were described to be down-regulated in the infected samples, particularly in the in vitro infection, such as miR-125b-5p, miR-99b-5p, miR-100 and miR-2887, suggesting that viral mechanisms can affect host miRNA expression. [score:6]
In the in vitro infection, miR-23a-3p was the most expressed miRNA representing the 50% of annotated reads, while miR-125b-5p was the most expressed miRNA in the in vivo infection, in both olfactory bulb and trigeminal ganglia, and only represented the 25% of the annotated reads. [score:5]
Looking at most abundant miRNAs (CN>100), we observed a clear predominance of those miRNAs over-expressed in mock-infected group (Table 4), such as miR-125b-5p, miR-99b-5p and miR-100. [score:3]
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[+] score: 9
Of these, 40 miRNAs are minimally expressed (0 < average signals ≤ 100; p ≤ 0.01), 77 miRNAs are modestly expressed 100 < average signals ≤ 1,000; p ≤ 0.01), 85 miRNAs were highly expressed (1,000 < average signals ≤ 10,000), and, in particular, 20 miRNAs were extremely highly expressed in the anterior pituitary (average signals ≥ 10,000; p ≤ 0.01), including ssc-miR-7, Y-90, ssc-miR-26a, ssc-miR-125b, Y-1, ssc-miR-125a, Y-77, ssc-let-7g, ssc-miR-29a, ssc-let-7i, ssc-let-7a, ssc-let-7f, ssc-miR-148a, ssc-miR-21, ssc-miR-335, ssc-miR-30b-5p, ssc-miR-191, ssc-miR-29c, ssc-miR-23b, and ssc-miR-23a (Fig 1C). [score:9]
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[+] score: 9
For example, between E35 and E45, miR-125 was the significantly differentially expressed miRNA (p<0.01), as the expression level was very high, this may be the key miRNAs in this stage. [score:5]
Seven key miRNAs including let-7f, miR-125b, miR-133a, miR-199a, miR-200b, miR-200c and miR-455 are highly expressed in the mesenchyme or epithelium of different tooth development stages, but their functions have not been elucidated [6], [8]. [score:4]
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[+] score: 7
The summary of the six DE miRNA common to all species is described in Fig.   5. Briefly, all DE candidates were single copy miRNA across all libraries, and 4 DE miRNA (miR-101-3p, miR-16-5p, miR-143-3p and miR-155-5p) were up-regulated in bats while 2 (miR-125-5p and miR-221-5p) were down-regulated. [score:7]
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[+] score: 7
For example, we found that the expressions of ssc-miR-26a and ssc-miR-125b were much higher than their expressions reported in the previous study [40]. [score:5]
Thus, ssc-miR-26a and ssc-miR-125b may play vital roles in the regulation of skeletal muscle postnatal hypertrophy. [score:2]
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[+] score: 6
The unified set of top 10 unique miRNAs over the two pig breeds correspond to 15 unique miRNAs, 11 of which (ssc-let-7a-1/2-5p, ssc-let-7c-5p, ssc-let-7e-5p, ssc-miR-10a-5p, ssc-miR-10b-5p, ssc-miR-127-3p, ssc-miR-148a-3p, ssc-miR-199a-1/2-5p, ssc-miR-21-5p, ssc-miR-26a-5p, ssc-miR-125b-1-5p) had been frequently reported highly expressed in skeletal muscle during porcine prenatal and postnatal developmental stages. [score:4]
MiR-125b negatively modulates myoblast differentiation in culture and muscle regeneration in mice by targeting IGF-II [29]. [score:2]
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[+] score: 6
miR-23 inhibits PRRSV replication by targeting PRRSV RNA [16], while miR-125b reduces PRRSV replication by negatively regulating the NF-κB pathway [17]. [score:6]
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[+] score: 4
Other miRNAs from this paper: hsa-let-7a-1, hsa-let-7a-2, hsa-let-7a-3, hsa-let-7b, hsa-let-7c, hsa-let-7d, hsa-let-7e, hsa-let-7f-1, hsa-let-7f-2, hsa-mir-15a, hsa-mir-17, hsa-mir-21, hsa-mir-24-1, hsa-mir-24-2, hsa-mir-27a, hsa-mir-30a, hsa-mir-103a-2, hsa-mir-103a-1, hsa-mir-107, mmu-let-7g, mmu-let-7i, mmu-mir-27b, mmu-mir-30a, mmu-mir-30b, mmu-mir-125b-2, mmu-mir-9-2, mmu-mir-150, mmu-mir-24-1, mmu-mir-204, hsa-mir-30c-2, hsa-mir-30d, mmu-mir-30e, hsa-mir-204, hsa-mir-210, hsa-mir-221, hsa-mir-222, mmu-let-7d, hsa-let-7g, hsa-let-7i, hsa-mir-27b, hsa-mir-30b, hsa-mir-125b-1, hsa-mir-9-1, hsa-mir-9-2, hsa-mir-9-3, hsa-mir-125b-2, hsa-mir-150, mmu-mir-30c-1, mmu-mir-30c-2, mmu-mir-30d, mmu-let-7a-1, mmu-let-7a-2, mmu-let-7b, mmu-let-7c-1, mmu-let-7c-2, mmu-let-7e, mmu-let-7f-1, mmu-let-7f-2, mmu-mir-15a, mmu-mir-21a, mmu-mir-24-2, mmu-mir-27a, mmu-mir-103-1, mmu-mir-103-2, mmu-mir-326, mmu-mir-107, mmu-mir-17, mmu-mir-210, mmu-mir-221, mmu-mir-222, mmu-mir-9-1, mmu-mir-9-3, mmu-mir-125b-1, hsa-mir-30c-1, hsa-mir-30e, hsa-mir-378a, mmu-mir-378a, hsa-mir-326, ssc-mir-125b-2, ssc-mir-24-1, ssc-mir-326, ssc-mir-27a, ssc-let-7c, ssc-let-7f-1, ssc-let-7i, ssc-mir-103-1, ssc-mir-107, ssc-mir-204, ssc-mir-21, ssc-mir-30c-2, ssc-mir-9-1, ssc-mir-9-2, hsa-mir-378d-2, hsa-mir-103b-1, hsa-mir-103b-2, ssc-mir-15a, ssc-mir-17, ssc-mir-30b, ssc-mir-210, ssc-mir-221, ssc-mir-30a, ssc-let-7a-1, ssc-let-7e, ssc-let-7g, ssc-mir-378-1, ssc-mir-30d, ssc-mir-30e, ssc-mir-103-2, ssc-mir-27b, ssc-mir-24-2, ssc-mir-222, hsa-mir-378b, hsa-mir-378c, ssc-mir-30c-1, ssc-mir-378-2, hsa-mir-378d-1, hsa-mir-378e, hsa-mir-378f, hsa-mir-378g, hsa-mir-378h, hsa-mir-378i, mmu-mir-378b, ssc-let-7a-2, hsa-mir-378j, mmu-mir-21b, mmu-let-7j, mmu-mir-378c, mmu-mir-21c, mmu-mir-378d, mmu-mir-30f, ssc-let-7d, ssc-let-7f-2, ssc-mir-9-3, ssc-mir-150-1, ssc-mir-150-2, mmu-let-7k, ssc-mir-378b, mmu-mir-9b-2, mmu-mir-9b-1, mmu-mir-9b-3
We found 13 adipogenesis-promoting miRNAs (let-7、miR-9、miR-15a、miR-17、miR-21、miR-24、miR-30、miR-103、miR-107、miR-125b、miR-204、miR-210、and miR-378) target 860 lncRNA loci. [score:3]
We analyzed the relationship between the 343 identified lncRNAs with the 13 promoting adipogenesis miRNAs (let-7、miR-9、miR-15a、miR-17、miR-21、miR-24、miR-30、miR-103、miR-107、miR-125b、miR-204、miR-210、and miR-378) and five depressing adipogenesis miRNAs (miR-27, miR-150, miR-221, miR-222, and miR-326). [score:1]
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[+] score: 3
Other miRNAs from this paper: ssc-mir-122, ssc-mir-125b-2, ssc-mir-181b-2, ssc-mir-20a, ssc-mir-23a, ssc-mir-26a, ssc-mir-29b-1, ssc-mir-181c, ssc-mir-214, ssc-let-7c, ssc-let-7f-1, ssc-let-7i, ssc-mir-103-1, ssc-mir-107, ssc-mir-21, ssc-mir-29c, ssc-mir-30c-2, bta-mir-26a-2, bta-mir-29a, bta-let-7f-2, bta-mir-103-1, bta-mir-20a, bta-mir-21, bta-mir-26b, bta-mir-30d, bta-mir-499, bta-mir-99a, bta-mir-125b-1, bta-mir-126, bta-mir-181a-2, bta-mir-199a-1, bta-mir-30b, bta-mir-107, bta-mir-10a, bta-mir-127, bta-mir-142, bta-mir-181b-2, bta-mir-30e, bta-mir-92a-2, bta-let-7d, bta-mir-132, bta-mir-138-2, bta-mir-17, bta-mir-181c, bta-mir-192, bta-mir-199b, bta-mir-200a, bta-mir-200c, bta-mir-214, bta-mir-23a, bta-mir-29b-2, bta-mir-29c, bta-mir-455, bta-let-7g, bta-mir-10b, bta-mir-30a, bta-mir-200b, bta-let-7a-1, bta-let-7f-1, bta-mir-122, bta-mir-30c, bta-let-7i, bta-mir-25, bta-let-7a-2, bta-let-7a-3, bta-let-7b, bta-let-7c, bta-let-7e, bta-mir-103-2, bta-mir-125b-2, bta-mir-99b, ssc-mir-99b, ssc-mir-17, ssc-mir-30b, ssc-mir-199b, bta-mir-1-2, bta-mir-1-1, bta-mir-129-1, bta-mir-129-2, bta-mir-133a-2, bta-mir-133a-1, bta-mir-133b, bta-mir-135b, bta-mir-138-1, bta-mir-143, bta-mir-144, bta-mir-146b, bta-mir-146a, bta-mir-181d, bta-mir-190a, bta-mir-199a-2, bta-mir-202, bta-mir-206, bta-mir-211, bta-mir-212, bta-mir-223, bta-mir-26a-1, bta-mir-29d, bta-mir-30f, bta-mir-338, bta-mir-33a, bta-mir-33b, bta-mir-375, bta-mir-429, bta-mir-451, bta-mir-92a-1, bta-mir-92b, bta-mir-29e, bta-mir-29b-1, bta-mir-181a-1, bta-mir-181b-1, ssc-mir-133a-1, ssc-mir-1, ssc-mir-146b, ssc-mir-181a-1, ssc-mir-30a, bta-mir-199c, ssc-mir-206, ssc-let-7a-1, ssc-let-7e, ssc-let-7g, ssc-mir-133b, ssc-mir-29a, ssc-mir-30d, ssc-mir-30e, ssc-mir-199a-2, ssc-mir-499, ssc-mir-143, ssc-mir-10a, ssc-mir-10b, ssc-mir-103-2, ssc-mir-181a-2, ssc-mir-181b-1, ssc-mir-181d, ssc-mir-99a, ssc-mir-92a-2, ssc-mir-92a-1, ssc-mir-92b, ssc-mir-192, ssc-mir-142, ssc-mir-127, ssc-mir-202, ssc-mir-129a, ssc-mir-455, ssc-mir-338, ssc-mir-133a-2, ssc-mir-146a, bta-mir-26c, ssc-mir-30c-1, ssc-mir-126, ssc-mir-199a-1, ssc-mir-451, ssc-let-7a-2, ssc-mir-129b, ssc-mir-429, ssc-let-7d, ssc-let-7f-2, ssc-mir-29b-2, ssc-mir-132, ssc-mir-138, ssc-mir-144, ssc-mir-190a, ssc-mir-212, bta-mir-133c, ssc-mir-26b, ssc-mir-200b, ssc-mir-223, ssc-mir-375, ssc-mir-33b
Skaftnesmo et al. (2017) explored which miRNAs regulate mRNAs during initiation of puberty, and several regulated miRNAs in the pubertal stage had earlier been associated (miR-20a, miR-25, miR-181a, miR-202, let7c/d/a, miR-125b, miR-222a/b, miR-190a) or have now been found connected (miR-2188, miR-144, miR-731, miR-8157) to the initiation of puberty. [score:3]
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[+] score: 3
The expression of miR-23a, miR-23b, and miR-24 was significantly reduced following pacing, while that of miR-133a, miR-125-3p, and miR-141 remained unchanged. [score:3]
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[+] score: 3
Wang Y. -D. Cai N. Wu X. Cao H. Xie L. Zheng P. OCT4 promotes tumorigenesis and inhibits apoptosis of cervical cancer cells by miR-125b/BAK1 pathway Cell Death Dis. [score:3]
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[+] score: 3
However, it should be noted that a single miRNA, for example such as ssc-miR-103-2, ssc-miR-27b, ssc-miR-23b, and ssc-miR-125b-1, may have multiple precursor targeting regions in the genome. [score:3]
[1 to 20 of 1 sentences]
[+] score: 3
Unfortunately, we did not get mRNA target for some miRNAs, such as miR-106b and miRNA-125b in Landrace. [score:3]
[1 to 20 of 1 sentences]
[+] score: 3
0024883.g002 Figure 2 The selected miRNAs for the analysis include: miR-99b, miR-204, miR-27a, miR-24, miR-7, miR-145, miR-124, miR-21, miR-125b, miR-30b, miR-128a, miR-122, miR-183, and miR-103. [score:1]
0024883.g003 Figure 3 The selected miRNAs for the analysis include: miR-99b, miR-204, miR-27a, miR-24, miR-7, miR-145, miR-124, miR-21, miR-125b, miR-30b, miR-128a, miR-122, miR-183, and miR-103. [score:1]
The selected miRNAs for the analysis include: miR-99b, miR-204, miR-27a, miR-24, miR-7, miR-145, miR-124, miR-21, miR-125b, miR-30b, miR-128a, miR-122, miR-183, and miR-103. [score:1]
[1 to 20 of 3 sentences]
[+] score: 3
Other miRNAs from this paper: hsa-let-7a-1, hsa-let-7a-2, hsa-let-7a-3, hsa-let-7f-1, hsa-let-7f-2, hsa-mir-15a, hsa-mir-16-1, hsa-mir-21, hsa-mir-23a, hsa-mir-24-1, hsa-mir-24-2, hsa-mir-26a-1, hsa-mir-29a, hsa-mir-30a, hsa-mir-31, hsa-mir-99a, hsa-mir-29b-1, hsa-mir-29b-2, hsa-mir-103a-2, hsa-mir-103a-1, hsa-mir-16-2, hsa-mir-192, hsa-mir-148a, hsa-mir-10b, hsa-mir-181a-2, hsa-mir-181a-1, hsa-mir-215, hsa-mir-223, hsa-mir-224, hsa-mir-200b, hsa-mir-15b, hsa-mir-27b, hsa-mir-125b-1, hsa-mir-141, hsa-mir-143, hsa-mir-152, hsa-mir-125b-2, hsa-mir-126, hsa-mir-146a, hsa-mir-184, hsa-mir-200c, hsa-mir-155, hsa-mir-29c, hsa-mir-200a, hsa-mir-99b, hsa-mir-296, hsa-mir-30e, hsa-mir-26a-2, hsa-mir-378a, hsa-mir-342, hsa-mir-148b, hsa-mir-451a, ssc-mir-125b-2, ssc-mir-148a, ssc-mir-15b, ssc-mir-184, ssc-mir-224, ssc-mir-23a, ssc-mir-24-1, ssc-mir-26a, ssc-mir-29b-1, ssc-let-7f-1, ssc-mir-103-1, ssc-mir-21, ssc-mir-29c, hsa-mir-486-1, hsa-mir-499a, hsa-mir-671, hsa-mir-378d-2, bta-mir-26a-2, bta-mir-29a, bta-let-7f-2, bta-mir-103-1, bta-mir-148a, bta-mir-16b, bta-mir-21, bta-mir-499, bta-mir-99a, bta-mir-125b-1, bta-mir-126, bta-mir-181a-2, bta-mir-27b, bta-mir-31, bta-mir-15b, bta-mir-215, bta-mir-30e, bta-mir-148b, bta-mir-192, bta-mir-200a, bta-mir-200c, bta-mir-23a, bta-mir-29b-2, bta-mir-29c, bta-mir-10b, bta-mir-24-2, bta-mir-30a, bta-mir-200b, bta-let-7a-1, bta-mir-342, bta-let-7f-1, bta-let-7a-2, bta-let-7a-3, bta-mir-103-2, bta-mir-125b-2, bta-mir-15a, bta-mir-99b, hsa-mir-664a, ssc-mir-99b, hsa-mir-103b-1, hsa-mir-103b-2, ssc-mir-15a, ssc-mir-16-2, ssc-mir-16-1, bta-mir-141, bta-mir-143, bta-mir-146a, bta-mir-152, bta-mir-155, bta-mir-16a, bta-mir-184, bta-mir-24-1, bta-mir-223, bta-mir-224, bta-mir-26a-1, bta-mir-296, bta-mir-29d, bta-mir-378-1, bta-mir-451, bta-mir-486, bta-mir-671, bta-mir-29e, bta-mir-29b-1, bta-mir-181a-1, ssc-mir-181a-1, ssc-mir-215, ssc-mir-30a, bta-mir-2318, bta-mir-2339, bta-mir-2430, bta-mir-664a, bta-mir-378-2, ssc-let-7a-1, ssc-mir-378-1, ssc-mir-29a, ssc-mir-30e, ssc-mir-499, ssc-mir-143, ssc-mir-10b, ssc-mir-486-1, ssc-mir-152, ssc-mir-103-2, ssc-mir-181a-2, ssc-mir-27b, ssc-mir-24-2, ssc-mir-99a, ssc-mir-148b, ssc-mir-664, ssc-mir-192, ssc-mir-342, oar-mir-21, oar-mir-29a, oar-mir-125b, oar-mir-181a-1, hsa-mir-378b, hsa-mir-378c, ssc-mir-296, ssc-mir-155, ssc-mir-146a, bta-mir-148c, ssc-mir-126, ssc-mir-378-2, ssc-mir-451, hsa-mir-378d-1, hsa-mir-378e, hsa-mir-378f, hsa-mir-378g, hsa-mir-378h, hsa-mir-378i, hsa-mir-451b, hsa-mir-499b, ssc-let-7a-2, ssc-mir-486-2, hsa-mir-664b, hsa-mir-378j, ssc-let-7f-2, ssc-mir-29b-2, ssc-mir-31, ssc-mir-671, bta-mir-378b, bta-mir-378c, hsa-mir-486-2, oar-let-7a, oar-let-7f, oar-mir-103, oar-mir-10b, oar-mir-143, oar-mir-148a, oar-mir-152, oar-mir-16b, oar-mir-181a-2, oar-mir-200a, oar-mir-200b, oar-mir-200c, oar-mir-23a, oar-mir-26a, oar-mir-29b-1, oar-mir-30a, oar-mir-99a, bta-mir-664b, chi-let-7a, chi-let-7f, chi-mir-103, chi-mir-10b, chi-mir-125b, chi-mir-126, chi-mir-141, chi-mir-143, chi-mir-146a, chi-mir-148a, chi-mir-148b, chi-mir-155, chi-mir-15a, chi-mir-15b, chi-mir-16a, chi-mir-16b, chi-mir-184, chi-mir-192, chi-mir-200a, chi-mir-200b, chi-mir-200c, chi-mir-215, chi-mir-21, chi-mir-223, chi-mir-224, chi-mir-2318, chi-mir-23a, chi-mir-24, chi-mir-26a, chi-mir-27b, chi-mir-296, chi-mir-29a, chi-mir-29b, chi-mir-29c, chi-mir-30a, chi-mir-30e, chi-mir-342, chi-mir-378, chi-mir-451, chi-mir-499, chi-mir-671, chi-mir-99a, chi-mir-99b, bta-mir-378d, ssc-mir-378b, oar-mir-29b-2, ssc-mir-141, ssc-mir-200b, ssc-mir-223, bta-mir-148d
A differential expression of four immune related miRNAs, miR-125b, miR-155, miR-146a, and miR-223 upon stimulation of bovine monocytes with LPS or Staphylococcus aureus enterotoxin B was demonstrated (Dilda et al., 2012). [score:3]
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[+] score: 2
Other miRNAs from this paper: hsa-let-7a-1, hsa-let-7a-2, hsa-let-7a-3, hsa-let-7b, hsa-let-7c, hsa-let-7d, hsa-let-7e, hsa-let-7f-1, hsa-let-7f-2, hsa-mir-17, hsa-mir-23a, hsa-mir-24-1, hsa-mir-24-2, hsa-mir-26a-1, hsa-mir-27a, hsa-mir-29a, hsa-mir-29b-1, hsa-mir-29b-2, hsa-mir-103a-2, hsa-mir-103a-1, hsa-mir-199a-1, hsa-mir-208a, hsa-mir-148a, hsa-mir-10a, hsa-mir-181a-2, hsa-mir-181c, hsa-mir-199a-2, hsa-mir-181a-1, hsa-mir-214, hsa-mir-221, hsa-let-7g, hsa-let-7i, hsa-mir-1-2, hsa-mir-23b, hsa-mir-27b, hsa-mir-125b-1, hsa-mir-128-1, hsa-mir-133a-1, hsa-mir-133a-2, hsa-mir-143, hsa-mir-125b-2, hsa-mir-126, hsa-mir-127, hsa-mir-206, hsa-mir-1-1, hsa-mir-128-2, hsa-mir-29c, hsa-mir-26a-2, hsa-mir-378a, hsa-mir-148b, hsa-mir-133b, hsa-mir-424, ssc-mir-125b-2, ssc-mir-148a, ssc-mir-23a, ssc-mir-24-1, ssc-mir-26a, ssc-mir-29b-1, ssc-mir-181c, ssc-mir-214, ssc-mir-27a, ssc-let-7c, ssc-let-7f-1, ssc-let-7i, ssc-mir-103-1, ssc-mir-128-1, ssc-mir-29c, hsa-mir-486-1, hsa-mir-499a, hsa-mir-503, hsa-mir-411, hsa-mir-378d-2, hsa-mir-208b, hsa-mir-103b-1, hsa-mir-103b-2, ssc-mir-17, ssc-mir-221, ssc-mir-133a-1, ssc-mir-1, ssc-mir-503, ssc-mir-181a-1, ssc-mir-206, ssc-let-7a-1, ssc-let-7e, ssc-let-7g, ssc-mir-378-1, ssc-mir-133b, ssc-mir-29a, ssc-mir-199a-2, ssc-mir-128-2, ssc-mir-499, ssc-mir-143, ssc-mir-10a, ssc-mir-486-1, ssc-mir-103-2, ssc-mir-181a-2, ssc-mir-27b, ssc-mir-24-2, ssc-mir-23b, ssc-mir-148b, ssc-mir-208b, ssc-mir-424, ssc-mir-127, hsa-mir-378b, hsa-mir-378c, ssc-mir-411, ssc-mir-133a-2, ssc-mir-126, ssc-mir-199a-1, ssc-mir-378-2, hsa-mir-378d-1, hsa-mir-378e, hsa-mir-378f, hsa-mir-378g, hsa-mir-378h, hsa-mir-378i, hsa-mir-499b, ssc-let-7a-2, ssc-mir-486-2, hsa-mir-378j, ssc-let-7d, ssc-let-7f-2, ssc-mir-29b-2, hsa-mir-486-2, ssc-mir-378b
In addition to the best-studied myomiRs (miR-1, -206 and miR-133 families), 11 other DE muscle-related miRNAs (miR-378 [24], miR-148a [27], miR-26a [28, 29], miR-27a/b [30, 31], miR-23a [32, 33], miR-125b [34], miR-24 [35], miR-128 [36], miR-199a [37] and miR-424 [38]) with high abundance (average RPM >1,000) and another 14 (miR-181a/b/c/d-5p [26], miR-499-5p [11], miR-503 [38], miR-486 [39], miR-214 [40], miR-29a/b/c [41– 43], miR-221/222 [44] and miR-208 [11] with low abundance (average RPM <1,000) were detected in myogenesis of pig. [score:1]
However, Cluster 5 illustrated that ssc-miR-206 and other four muscle-related miRNAs (ssc-miR-126, -148a/b and -15b) continued to decline while ssc-miR-133b and eleven other muscle-related miRNAs (ssc-miR-125b, -128,-181a/b, -199a, -214, -23a, -24, -424, -503 and -7) in Cluster 4 presented a down and then up trend from 77 dpc to 180 dpn, suggesting their different roles played in adult fiber maturation. [score:1]
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[+] score: 1
Other miRNAs from this paper: ssc-mir-125b-2
MiR-125b reduces porcine reproductive and respiratory syndrome virus replication by negatively regulating the NF-κB pathway. [score:1]
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[+] score: 1
The first one harbored known miRNAs such as miR-26a, miR-27a, miR-125b, miR-130a and miR-145 but the latter was mainly composed of novel and not conserved miRNAs. [score:1]
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